We then investigated a possible role for endogenously formed KOR ligands to regulate basal synaptic transmission in CeA by applying norBNI alone onto slices. Superfusion of 0.2 μM norBNI markedly augmented IPSPs in 75% of the neurons (12 of 16; Fig. 4A). On average, norBNI significantly increased inhibitory transmission to 136 ± 4% of pre-drug value after 10 min of application (n = 12, t = 6.438; Fig. 4B). The KOR antagonist concomitantly decreased the paired-pulse ratio in a significant manner to 77 ± 8% of control value (n = 12, t = 3.215; Fig. 4C), from 1.16 ± 0.07 before norBNI to 0.89 ± 0.09 in the presence of the antagonist, indicating increased GABA release upon blockade of KOR. The augmentation of IPSPs upon blockade of KOR by norBNI is likely due to the prevention of basal activity exerted by endogenously formed dynorphin. These data suggest that endogenously formed KOR ligands tonically regulate inhibitory transmission in CeA by decreasing the release of GABA.
